Skip to main content.

Subhrajit Saha, Ph.D., M.Tech, MSc

Subhrajit Saha portrait
Professor, Radiation Oncology

Graduate Faculty, Cancer Biology

Graduate Faculty, Cancer Biology

ssaha@kumc.edu

Professional Background

Dr. Saha received his M.Tech in Biotechnology and Biochemical Engineering from Indian Institute of Technology KGP (2001) and his Ph.D. from Jadavpur University (2006), India. Dr. Saha completed his Post Doctoral education in Department of Radiation Oncology at Albert Einstein College of Medicine where he became an Assistant Professor and started his research group in 2013. He joined KUMC in 2016 as an Assistant Professor in Department of Radiation Oncology. In 2019, he was promoted with tenure to Associate Professor in the Department of Radiation Oncology. He is a member of the KU Cancer Center and has a secondary appointment in the Department of Cancer Biology and Department of Pathology andamp; Laboratory Medicine.

Dr. Saha's research focuses on cancer therapeutics and improvement in survival of cancer patients undergoing radiotherapy. The eventual goal of his research is to develop novel therapeutic strategies to increase the efficacy of radiotherapy by radio-sensitizing the malignant tissue along with ameliorating the radiation toxicity on normal tissue. His laboratory is also involved in development of medical countermeasures against radiological/nuclear accidents or terrorism.

Education and Training
  • PhD, Life Science & Biotechnology, Jadavpur University, India
  • Other, Biotechnology & Biochemical Engineering, Indian Institute of Technology, KGP, India, KGP, India
  • MSC, Physiology, University of Calcutta, India
  • BSc, Physiology Hons., University of Calcutta, India
Professional Affiliations
  • American Cancer Society, American Cancer Society Institutional Research Grant Review Committee, Member, 2017 - 2020
  • American Society of Therapeutic Radiation Oncology, Member, 2017 - 2023
  • International Journal of Radiation Oncology Biology Physics, Reviewer, 2015 - 2023
  • Radiation Research Society, Member, 2010 - Present
  • American Association of Cancer Research, Member, 2008 - Present

Research

Overview

Trophic role of macrophages in regeneration and repair of intestinal stem cell
Intestinal injury is a limiting factor for definitive chemo-radiation therapy of abdominal malignancies, such as, gastric, pancreatic and colorectal cancer. Thus, tumoricidal doses of RT or chemotherapy are not administered in the treatment of abdominal tumors, resulting in poor survival and early metastatic spread. Intestinal injury limits the application of high dose stereotactic radiosurgery (SRS) in abdominal cancers. Using novel mice genetics and virus-based tools, Dr. Saha's group has already demonstrated that macrophage/myeloid population in intestinal stem cell niche is critical for intestinal epithelial homeostasis. Currently his lab is involved in identifying macrophage derived regenerative signal and specific phenotype of macrophages involved in intestinal repair following radiation injury. Overall goal is to design a macrophage directed therapy to ameliorate radiation toxicity in intestine.

Macrophages in colonic inflammation and malignancy
Pro-inflammatory macrophages promote the onset of malignancy by inducing stress-adaptive responses of the inflamed epithelium as well as cellular survival and self-renewal. The anti-inflammatory/tissue resident macrophages are primarily involved in invasion and metastasis. Dr. Saha's group is pursuing another project to determine origin, phenotype and mechanism of invasion of these macrophages in irradiated tumor tissue. The overall goal of this project is to develop candidate agents which can deplete these pro-malignant macrophages or modulate their recruitment to induce the radio-sensitivity of tumor tissue.

Precision Radiation: Development of Preclinical model to optimize personalized radiotherapy
Differences in radiosensitivity among individuals is a key determinant for successful therapy. Currently Dr. Saha’s lab is developing genetically modified mice model and human tissue derived organoid system to address key molecular mechanisms responsible for differences in radiosensitivity. These preclinical platforms will allow identification and validation of biomarkers to be used in designing personalized treatment.

Current Research and Grants
  • BCN057 as a mitigator of Radiation Induced Gastrointestinal Syndrome, NIH, Co-PI
Publications
  • Kasi, A, Allen, J, Mehta, K, Dandawate, P, Saha, S, Bossmann, S, Anant, S, Sun, W. 2021. Association of losartan with outcomes in metastatic pancreatic cancer patients treated with chemotherapy.. Journal of clinical and translational research, 7 (2), 257-262. https://www-ncbi-nlm-nih-gov.kumc.idm.oclc.org/pmc/articles/PMC8177858/
  • Nag, D, Bhanja, P, Riha, R, Sanchez-Guerrero, G, Kimler, B., F, Tsue, T., T, Lominska, C, Saha, S. 2019. Auranofin Protects Intestine against Radiation Injury by Modulating p53/p21 Pathway and Radiosensitizes Human Colon Tumor.. Clinical cancer research : an official journal of the American Association for Cancer Research, 25 (15), 4791-4807. https://www-ncbi-nlm-nih-gov.kumc.idm.oclc.org/pmc/articles/PMC9159899/
  • Bhanja, P, Norris, A, Gupta-Saraf, P, Hoover, A, Saha, S. 2018. BCN057 induces intestinal stem cell repair and mitigates radiation-induced intestinal injury.. Stem cell research & therapy, 9 (1), 26. https://www-ncbi-nlm-nih-gov.kumc.idm.oclc.org/pmc/articles/PMC5797353/
  • Saha, S, Bhanja, P, Kabarriti, R, Liu, L, Alfieri, A., A, Guha, C. 2011. Bone marrow stromal cell transplantation mitigates radiation-induced gastrointestinal syndrome in mice.. PloS one, 6 (9), e24072. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3174150/ | PMC3174150, | 21935373
  • Dandawate, P, Kaushik, G, Ghosh, C, Standing, D, Ali Sayed, A., A, Choudhury, S, Subramaniam, D, Manzardo, A, Banerjee, T, Santra, S, Ramamoorthy, P, Butler, M, Padhye, S., B, Baranda, J, Kasi, A, Sun, W, Tawfik, O, Coppola, D, Malafa, M, Umar, S, Soares, M., J, Saha, S, Weir, S., J, Dhar, A, Jensen, R., A, Thomas, S., M, Anant, S. 2020. Diphenylbutylpiperidine Antipsychotic Drugs Inhibit Prolactin Receptor Signaling to Reduce Growth of Pancreatic Ductal Adenocarcinoma in Mice.. Gastroenterology, 158 (5), 1433-1449.e27. https://pubmed-ncbi-nlm-nih-gov.kumc.idm.oclc.org/31786131/
  • Saha, S, Chowdhury, P, Pal, A, Chakrabarti, M., K. 2008. Downregulation of human colon carcinoma cell (COLO-205) proliferation through PKG-MAP kinase mediated signaling cascade by E. coli heat stable enterotoxin (STa), a potent anti-angiogenic and anti-metastatic molecule.. Journal of applied toxicology : JAT, 28 (4), 475-83. https://pubmed-ncbi-nlm-nih-gov.kumc.idm.oclc.org/17828804/
  • Chugh, R., M, Bhanja, P, Norris, A, Saha, S. 2021. Experimental Models to Study COVID-19 Effect in Stem Cells.. Cells, 10 (1). https://pubmed-ncbi-nlm-nih-gov.kumc.idm.oclc.org/33430424/
  • Yusuf, K, Saha, S, Umar, S. 2022. Health Benefits of Dietary Fiber for the Management of Inflammatory Bowel Disease.. Biomedicines, 10 (6). https://www-ncbi-nlm-nih-gov.kumc.idm.oclc.org/pmc/articles/PMC9220141/
  • Chugh, R., M, Bhanja, P, Olea, X., D, Tao, F, Schroeder, K, Zitter, R, Arora, T, Pathak, H, Kimler, B., F, Godwin, A., K, Perry, J., M, Saha, S. 2022. Human Peripheral Blood Mononucleocyte Derived Myeloid Committed Progenitor Cells Mitigate H-ARS by Exosomal Paracrine Signal.. International journal of molecular sciences, 23 (10). https://www-ncbi-nlm-nih-gov.kumc.idm.oclc.org/pmc/articles/PMC9142131/
  • Kulkarni, S, Koller, A, Mani, K., M, Wen, R, Alfieri, A, Saha, S, Wang, J, Patel, P, Bandeira, N, Guha, C, Chen, E., I. 2016. Identifying Urinary and Serum Exosome Biomarkers for Radiation Exposure Using a Data Dependent Acquisition and SWATH-MS Combined Workflow.. International journal of radiation oncology, biology, physics, 96 (3), 566-77. https://www-ncbi-nlm-nih-gov.kumc.idm.oclc.org/pmc/articles/PMC5042854/